Category: physiology

Science conundrum of the day: why do we need to urinate when we hear running water?

August 29, 2025 • 9:40 am

I use a Water-Pik after flossing (and so should you!), and I’ve noticed repeatedly that when I am squirting water between my teeth, I develop a sudden urge to urinate.  Then I remembered the old summer-camp trick of putting a sleeping boy’s hands into a bowl of water, which supposedly made him wet his bed.  I think asked a few friends if they also had an urge to micturate when they heard running water, and to a person they said “yes.” (One emphasized the need to pee in the shower.)

Well, immediately this brings up a question: “why does this happen?”  There are two ways to approach this question.

First, there’s the physiological or “proximal” approach, which asks, “What is the neuronal/physiological basis of having to pee when you hear running water?”  This question is in principle answerable, and, as you’ll see, appears to have been answered.

But there’s the evolutionary or “ultimate” approach. If one assumes this connection between water and urination arose directly via natural selection (and remember, it could be fortuitous: simply a byproduct of how our bodies evolved), why is it adaptive to respond to the sound of running water this way?

This question may not be answerable, as we weren’t around to see when it happens. (One could I suppose, at least see if the connection exists in other primates, which would bnttress the fact that it arose in a common ancestor and has persisted, but doesn’t answer whether the connection evolved directly by natural selection.)

These are two different ways of thinking about the question: the “how” approach versus the “why” approach.  As I said, the “how” appears to have an answer in humans, as evidenced in this article from Australia’s Swinburn University (click to read):

First of all, the article asserts that the urge to pee when you hear running water is widespread, and occurs not just in the presence of water. (I haven’t had “nervous wees” before a date, though.)

We all know that feeling when nature calls – but what’s far less understood is the psychology behind it. Why, for example, do we get the urge to pee just before getting into the shower, or when we’re swimming? What brings on those “nervous wees” right before a date?

But let’s take a readers’ poll to see how widespread it is. Remember, your answer is anonymous, so please answer:

Do you get the urge to urinate when you hear or see water, running or not?

View Results

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Now, the “how” answer as given in the article above:

Research suggests our brain and bladder are in constant communication with each other via a neural network called the brain-bladder axis.

This complex web of circuitry is comprised of sensory neural activity, including the sympathetic and parasympathetic nervous systems. These neural connections allow information to be sent back and forth between the brain and bladder.

The brain-bladder axis not only facilitates the act of peeing, but is also responsible for telling us we need to go in the first place.

How do we know when we need to go?

As the bladder fills with urine and expands, this activates special receptors detecting stretch in the nerve-rich lining of the bladder wall. This information is then relayed to the “periaqueductal gray” – a part of the brain in the brainstem which constantly monitors the bladder’s filling status.

Once the bladder reaches a certain threshold (roughly 250-300ml of urine), another part of the brain called the “pontine micturition centre” is activated and signals that the bladder needs to be emptied. We, in turn, register this as that all-too-familiar feeling of fullness and pressure down below.

Beyond this, however, a range of situations can trigger or exacerbate our need to pee, by increasing the production of urine and/or stimulating reflexes in the bladder.

An illustration of where the brain’s “bladder control center”:

The periaqueductal gray is a section of gray matter located in the midbrain section of the brainstem. The periaqueductal gray is a section of gray matter located in the midbrain section of the brainstem. Image: Wikimedia/OpenStax, CC BY-SA

There’s more:

Peeing in the shower:

If you’ve ever felt the need to pee while in the shower (no judgement here) it may be due to the sight and sound of running water.

In a 2015 study, researchers demonstrated that males with urinary difficulties found it easier to initiate peeing when listening to the sound of running water being played on a smartphone.

Symptoms of overactive bladder, including urgency (a sudden need to pee), have also been linked to a range of environmental cues involving running water, including washing your hands and taking a shower.

This is likely due to both physiology and psychology. Firstly, the sound of running water may have a relaxing physiological effect, increasing activity of the parasympathetic nervous system. This would relax the bladder muscles and prepare the bladder for emptying.

At the same time, the sound of running water may also have a conditioned psychological effect. Due to the countless times in our lives where this sound has coincided with the actual act of peeing, it may trigger an instinctive reaction in us to urinate.

This would happen in the same way Pavlov’s dog learnt, through repeated pairing, to salivate when a bell was rung.

I’m not sure that a physiological effect differs from a psychological effect, except that the latter would be “learned” rather than inborn. But remember that any physiological effect like this has to come in through the senses and brain, which could be seen as “psychological”.

More “how” answers, involving different mechanisms:

But it’s not just the sight or sound of running water that makes us want to pee. Immersion in cold water has been shown to cause a “cold shock response”, which activates the sympathetic nervous system.

This so-called “fight or flight” response drives up our blood pressure which, in turn, causes our kidneys to filter out more fluid from the bloodstream to stabilise our blood pressure, in a process called “immersion diuresis”. When this happens, our bladder fills up faster than normal, triggering the urge to pee.

Interestingly, immersion in very warm water (such as a relaxing bath) may also increase urine production. In this case, however, it’s due to activation of the parasympathetic nervous system. One study demonstrated an increase in water temperature from 40℃ to 50℃ reduced the time it took for participants to start urinating.

or:

But it’s not just the sight or sound of running water that makes us want to pee. Immersion in cold water has been shown to cause a “cold shock response”, which activates the sympathetic nervous system.

This so-called “fight or flight” response drives up our blood pressure which, in turn, causes our kidneys to filter out more fluid from the bloodstream to stabilise our blood pressure, in a process called “immersion diuresis”. When this happens, our bladder fills up faster than normal, triggering the urge to pee.

Interestingly, immersion in very warm water (such as a relaxing bath) may also increase urine production. In this case, however, it’s due to activation of the parasympathetic nervous system. One study demonstrated an increase in water temperature from 40℃ to 50℃ reduced the time it took for participants to start urinating.

Conclusions:

We all pee (most of us several times a day). Yet research has shown about 75% of adults know little about how this process actually works – and even less about the brain-bladdder axis and its role in urination.

Well, you know now! More:

Most Australians will experience urinary difficulties at some point in their lives, so if you ever have concerns about your urinary health, it’s extremely important to consult a healthcare professional.

And should you ever find yourself unable to pee, perhaps the sight or sound of running water, a relaxing bath or a nice swim will help with getting that stream to flow.

This article was originally published on The Conversation.

. . . and that’s pretty much the whole article. The word “evolution” does not appear in it at all, so the “why” question isn’t answered. The “fight or flight” explanation is purely mechanistic, and in that case the urge to urinate is simply a byproduct of what happens when we’re frightened or angry.  But the rest—the sudden need to pee when you hear , see, or feel running water, remains unaddressed.

 

The mechanistic explanation also predicts that if you’re in a restroom and you hear other people peeing, that would increase your urge to join them.

As I said, the water-urination response may not be a direct response to natural selection. That is, there may be no reproductive advantage to having to pee when you encounter water. It could simply be, as Gould and Lewontin called it, a “spandrel.”  But let’s engage in some “adaptive storytelling” here and think up ways the connection might have been adaptive.

There don’t seem to be many.  The first one that struck me was that, as noted above, a lot of people have bladder issues (only ones that occur before reproduction ceases can be considered).  If this is the case, and if retaining urine is bad for you. which it is, then anything that facilitates peeing when you have bladder issues would be adaptive. If you already have a physiological system in place for peeing when your bladder’s full, it might be easier to hijack this system in those with bladder issues by using the same stimulus: the sound of running fluid. (This presumes that the sound stimulates urination even in people without bladder issues, which is apparently does.) But somehow I’m not satisfied with this

I asked a colleague, who gave a response that sounded good at the time but now seems dubious as well. He said that if you hear running water, you have an opportunity to hydrate yourself by drinking, and running water is more likely to be clean water that is good to drink. But the connection between having to drink and having to pee is obscure to me.

A question, then, for readers:

So, if one assumes that the connection between water and urination is the result of natural selection, please tender your own theory. Even crazy theories should be given, because, after all, “evolution is cleverer than you are.”

Remember this old joke?

Are insects sentient?

June 25, 2023 • 9:45 am

The Oxford English Dictionary gives three relevant definitions of the adjective “sentient”:

a.) That feels or is capable of feeling; having the power or function of sensation or of perception by the senses.

b.) Conscious or percipient of something.

c.) Physiology. Of organs or tissues: Responsive to sensory stimuli.

(“Sentience” itself is defined only as “The condition or quality of being sentient, consciousness, susceptibility to sensation.”)

The question that the Scientific American article below asks (and for once it’s written by a scientist in this field) is whether insects fit the definition of the first two definitions: do they have feelings and sensations experiencing qualia like pain, joy, pleasure, or the sensation of “redness”?  Or are insects merely chitinous robots that are programmed by evolution to act (to us) as if they have feelings—programmed reactions that we anthropormophize as similar to our own sensations? After all, you can be “responsive to sensory stimuli” (the third sense above) without actually feeling the sensory stimuli the way humans do.

Answering the question of whether a bee or a fly is sentient in the first two senses, or has consciousness (the ability to be sentient and perceive stimuli), is difficult. Some would say it’s impossible. After all, we all know that we ourselves have consciousness  and feel pain and joy, because we experience those things personally. But can I prove that, say, another person is conscious? Not directly, because we can’t get inside their brains. We infer that they’re conscious because they tell us they are; they are physically constructed with the same neurons that give us consciousness; and they act as if they experience qualia.  It’s inference, but of a Bayesian sort, and the question has high priors.

But can we extend this to other species?  Chittka uses the example of dogs:

Although there is still no universally accepted, single experimental proof for pain experiences in any animal, common sense dictates that as we accumulate ever more pieces of evidence that insects can feel, the probability that they are indeed sentient increases. For example, if a dog with an injured paw whimpers, licks the wound, limps, lowers pressure on the paw while walking, learns to avoid the place where the injury happened and seeks out analgesics when offered, we have reasonable grounds to assume that the dog is indeed experiencing something unpleasant.

This is a Bayesian approach to the question, and it’s really the only way to go. Yes, I think it’s highly probable that dogs, and most mammals, feel pain. But what about insects, reptiles and amphibians? They certainly avoid unpleasant stimuli and gravitate towards pleasant ones, which you could interpret as feeling joy, pleasure, or pain, but do they feel these sensations? If you say that the behavior denotes sentience, well remember that protozoans do these things, too (see below).

I’m fully aware that philosophers of mind have probably discussed this issue at length, and I haven’t followed that literature, so my musings here may seem childish to these philosophers.  But this Sci. Am. article (click below to read, or find it archived here) is not written for philosophers of mind but for people like me: folks interested in science and wanting to see what’s happening in other fields.  I found the article quite interesting, and for me it slightly raised the probability that insects can feel pain. But the answer remains far from settled—or even of having a high probability. And the author admits that. But he cites a number of cool studies.

Here are the lines of evidence that, to Chittka, raise the Bayesian probability that insects have sentience: experiencing pain, pleasure, and even joy.

a.) They learn and can do really smart things. (All quotes from Chittka are indented):

The conventional wisdom about insects has been that they are automatons—unthinking, unfeeling creatures whose behavior is entirely hardwired. But in the 1990s researchers began making startling discoveries about insect minds. It’s not just the bees. Some species of wasps recognize their nest mates’ faces and acquire impressive social skills. For example, they can infer the fighting strengths of other wasps relative to their own just by watching other wasps fight among themselves. Ants rescue nest mates buried under rubble, digging away only over trapped (and thus invisible) body parts, inferring the body dimension from those parts that are visible above the surface. Flies immersed in virtual reality display attention and awareness of the passing of time. Locusts can visually estimate rung distances when walking on a ladder and then plan their step width accordingly (even when the target is hidden from sight after the movement is initiated).

All of these responses, of course, could come from computers programmed to learn from experience, which is exactly what we and other animals are. Natural selection has endowed us with a neuronal network that will make us behave in ways to further our reproduction (or, sometimes, that of our group—like an ant colony). We can program computers to do this, too: robots that avoid aversive stimuli and gravitate towards good ones. And clearly we behave in such a way that furthers our reproduction, of which survival is one component. But do insects experience the world, with its pleasures and pains, by having qualia similar to ours?

A related question is this: is consciousness like we have (feeling pain and joy) something that’s merely an epiphenomenon of having evolved a sufficiently complex nervous system, or is consciousness itself a product of natural selection to further our reproduction? We don’t know the answer, but it’s pretty clear that some of our conscious experiences, like pain, have evolved by selection. People who can’t feel pain as a result of neurological conditions or disease (like Hansen’s disease) quickly start getting infections, hurting their bodies without being aware, losing fingers, and the like. If you didn’t experience pain when putting your hand in boiling water, you’d damage your body. But if consciousness is just an epiphenomenon of a complex evolved nervous system, then we can’t automatically say that bees that act as if they’re conscious really are conscious.

I’m prepared to believe, based on what I said above, that mammals feel pain.  Maybe even reptiles or amphibians, though there are suggestions that fish don’t feel pain, at least in the way we do. All these creatures gravitate towards adaptive things and avoid nonadaptive ones, but again, they could be programmed to do so without the ancillary conscious experience that we have.

More evidence from Chittka:

b.) Insects act as if they can alter their consciousness:

Many plants contain bitter substances such as nicotine and caffeine to deter herbivores, but these substances are also found in low concentrations in some floral nectars. Researchers wondered whether pollinators might be deterred by such nectars, but they discovered the opposite. Bees actively seek out drugs such as nicotine and caffeine when given the choice and even self-medicate with nicotine when sick. Male fruit flies stressed by being deprived of mating opportunities prefer food containing alcohol (naturally present in fermenting fruit), and bees even show withdrawal symptoms when weaned off an alcohol-rich diet.

Again, seeking out things that are good for you, like curing you of illness or infection, could be programmed, either directly or as part of programs involved in “learning what gets rid of harmful conditions”. Now if bees are partial to coffee and cigarettes because it gets them high, then yes, it seems to show that they want to alter their consciousness, which implies that they have consciousness. But these facts aren’t that convincing to me, because nicotine and caffeine may have other beneficial physiological effects.

c.) Bees appear to be “optimistic”. Here’s the experiment Chittka adduces to support  that:

We trained one group of bees to associate the color blue with a sugary reward and green with no reward, and another group of bees to make the opposite association. We then presented the bees with a turquoise color, a shade intermediate between blue and green. A lucky subset of bees received a surprise sugar treat right before seeing the turquoise color; the other bees did not. The bees’ response to the ambiguous stimulus depended on whether they received a treat before the test: those that got the pretest sugar approached the intermediate color faster than those that didn’t.

The results indicate that when the bees were surprised with a reward, they experienced an optimistic state of mind. This state, which was found to be related to the neurotransmitter dopamine, made the bees more upbeat, if you will, about ambiguous stimuli—they approached it as they would the blue or green colors they were trained to associate with a reward.

This is not a meaningless experiment, but to me shows only that bees conditioned to approach a color after a sugar reward are more likely to approach something like that color than those who weren’t conditioned.  To call this “optimism” seems to me hyperbolically anthropomorphic.

d). Bees appear to experience “joy”.  This experiment is more suggestive to me:

Other work suggests that bees can experience not only optimism but also joy. Some years ago we trained bumblebees to roll tiny balls to a goal area to obtain a nectar reward—a form of object manipulation equivalent to human usage of a coin in a vending machine. In the course of these experiments, we noticed that some bees rolled the balls around even when no sugar reward was being offered. We suspected that this might be a form of play behavior.

Recently we confirmed this hunch experimentally. We connected a bumblebee colony to an arena equipped with mobile balls on one side, immobile balls on the other, and an unobstructed path through the middle that led to a feeding station containing freely available sugar solution and pollen. Bees went out of their way to return again and again to a “play area” where they rolled the mobile balls in all directions and often for extended periods without a sugar reward, even though plenty of food was provided nearby. There seemed to be something inherently enjoyable in the activity itself. In line with what other researchers have observed in vertebrate creatures at play, young bees engaged more often with the balls than older ones. And males played more than females (male bumblebees don’t work for the colony and therefore have a lot more time on their hands). These experiments are not merely cute—they provide further evidence of positive emotionlike states in bees.

It’s hard to understand these results without thinking that bees, like panda cubs, are playful, messing around with balls that give them pleasure. And since bees don’t experience balls in their natural state, they could be enjoying the novelty. On the other hand, they could simply be encountering something they haven’t experienced, and are following neuronal instructions to manipulate it to see how it operates, which could be useful knowledge in the future. This second interpretation means that no “pleasure” need be involved. Remember, play behavior in animals is often there to prepare them for what happens when they become adults, and isn’t just there for pleasure.

Again, it’s hard to judge from such studies whether bees are feeling pleasure in the way we do. But to me this makes it marginally more likely.

Finally,

e). Bees appear to weigh pain against pleasure, and change their behaviors when the balance is altered.  Here’s another experiment:

We decided to do an experiment with only moderately unpleasant stimuli, not injurious ones—and one in which bees could freely choose whether to experience these stimuli.

We gave bees a choice between two types of artificial flowers. Some were heated to 55 degrees Celsius (lower than your cup of coffee but still hot), and others were not. We varied the rewards given for visiting the flowers. Bees clearly avoided the heat when rewards for both flower types were equal. On its own, such a reaction could be interpreted as resulting from a simple reflex, without an “ouch-like” experience. But a hallmark of pain in humans is that it is not just an automatic, reflexlike response. Instead one may opt to grit one’s teeth and bear the discomfort—for example, if a reward is at stake. It turns out that bees have just this kind of flexibility. When the rewards at the heated flowers were high, the bees chose to land on them. Apparently it was worth their while to endure the discomfort. They did not have to rely on concurrent stimuli to make this trade-off. Even when heat and reward were removed from the flowers, bees judged the advantages and disadvantages of each flower type from memory and were thus able to make comparisons of the options in their minds.

To me, this really shows nothing more than that animals are attracted to adaptive stimuli and repelled by harmful ones, with the addition of being able to balance harms versus advantages. (This is like the “flight distance” of animals, with some individuals able to give more weight to attractive stimuli. That’s probably how cats got domesticated!) But it doesn’t tell us whether animals are feeling the pain or attraction the way we do.

And we should remember that even protozoans show avoidance of some external stimuli and can be induced by electrical shocks to avoid light. So these animals can be trained. Do they feel pain or pleasure? I doubt it—not protozoa!  They may not show “play” behavior, but perhaps they can be trained to weigh aversive versus adaptive stimuli, as in section “d” above.  I doubt anybody would conclude with confidence that protozoa feel pain the way we do (they don’t have a nervous system) or are even conscious.

Against the doubts that I’ve raised, Chittka offers a counterargument:

Critics could argue that each of the behaviors described earlier could also be programmed into a nonconscious robot. But nature cannot afford to generate beings that just pretend to be sentient. Although there is still no universally accepted, single experimental proof for pain experiences in any animal, common sense dictates that as we accumulate ever more pieces of evidence that insects can feel, the probability that they are indeed sentient increases.

The first sentence is what I have said already. And I’m willing to go along with the third sentence, too: as we learn more, the Bayesian probability that other species experience pain or pleasure can increase or decrease.

But I’m not willing to go along with the idea that “nature cannot afford to generate beings that just pretend to be sentient.”  What does he mean by “afford”? My interpretation is this: he’s saying that natural selection cannot produce organisms that act as if they’re sentient unless they really are sentient. And I cannot see any support for that, for we already know that protozoans act as if they experience qualia, but almost certainly don’t. And saying “pretend to be sentient” is pretty anthropormorphic! It implies, for example, that programmed robots that do what bees do are “pretending to be sentient” when in fact we know they are NOT sentient.

Finally, that leads to the Big AI Question: if we generate robots sufficiently complex that they respond exactly as humans do in complex situations requiring consciousness, does that mean that they have become conscious?  I say “no”, but others disagree.  After all, there are those panpsychists who say that even electrons and rocks have a rudimentary form of consciousness.

I’m writing this on the fly, so forgive me if my thoughts are half-baked.  I do think that Chtittka’s experiments are clever, and, over time, may give us a sense of sentience in other species. But I’m not yet ready to throw in with him on the claim that insects are conscious.  It’s enough for me now to realize that they do experience some aspects of the environment as things to be avoided. And that is why I have always anesthetized my fruit flies before killing them. (When I was an undergrad I used to take them to the biology department roof and let them go, but my advisor Bruce Grant nixed that on the grounds that I was polluting the natural gene pool of Drosophila.)

The last bit of Chittka’s paper is a thoughtful analysis of how these kinds of studies should condition our behavior towards insects. But even if they don’t feel pain, aversion or attraction itself should help us confect a philosophy of “insect ethics.”

h/t: Howard, who brought this paper to my attention and wanted my take on it. I’m sending him this link as my take.

Echidnas blow snot bubbles to keep their noses cool

January 23, 2023 • 11:15 am

You’ve heard about about platypuses, the monotreme egg-laying mammal that lays eggs, a primitive condition inherited from the ancestor of all modern mammals (and their earlier reptilian ancestors). But perhaps you also know of the “echidnas“, or “spiny anteaters” (not very related to regular anteaters), also in the order Monotremata and the only other egg-laying mammal. (These are not marsupials; they diverged from the placental/marsupial mammal group, called therians, between 250 and 160 million years ago.)

The living monotremes comprise four species of echidna and only one species of platypus (Ornithorhynchus anatinus), and these two groups diverged from each other between 57 and 21 million years ago. Further, the monotremes diverged from the “regular” (therian) mammals between 218 and 187 million years ago.

The article at hand is about one of the four echidna species, the short beaked-echidna (Tachyglossus aculeatus). Here’s what it looks like:

Click on the article below to read about how echidnas keep cool in the hot climate of Australia (the pdf is here, the full reference is at at bottom, and there’s a popular article here.  But the article below, from Biology Letters published by Britain’s Royal Society, is short and easy to read:

So the issue is this: earlier studies had demonstrated that this species had a low thermal tolerance, with a lethal core body temperature of 38ºC (100.4º F) and a lethal air temperature of just 35ºC (95º F). (From now on I’ll just give the Celsius temperatures, as you should get familiar with the conversion.) Yet the echidna is found in Australian habitats where the air temperature is higher than this, so they must have a way to cool off. The paper reports thermal-imaging studies of wild echidnas to see how they do this.

Clearly, the echidna must have some way to lower the temperature it encounters in the wild, which the authors call a “thermal window” or “regions of the animal’s body surface that vary heat exchange with the environment being ‘opened’ or ‘closed’ by changes in exposure and/or blood flow.” (Below are some cool examples of how other species do this.)

The authors measured the echidnas’ body temperature by thermal imaging, and estimated the ambient temperature as the average of the air temperature and tje ground temperature. They also measured a “wet bulb” temperature, which is the temperature measured by a wetted thermometer bulb. Wet-bulb temperature is cooler than the air temperature because the evaporation of the water from the bulb cools it off.

They found two ways that echidnas cool themselves off at higher temperatures. The temperature comparisons of echidna body parts with environmental temperature was measured by plotting, over a variety of echidnas observed at different temperatures, the wet bulb temperature (x axis) versus the surface temperature of the animal (y axis).  That’s shown below, but first one observation.

The first way of cooing the authors found was seeing the animals press their relatively furless (and spineless) inner leg an belly surfaces against the cool soil.  This is similar to what kangaroos do; see below. The spines also help keep the sun off their bodies, and there is a subcutaneous fat layer, into which the spines are embedded, that also provides insulation.

The second way of cooling is the swell finding given in the headline. You can see it below in the lower right section of the following graph. It shows body temperatures versus wet bulb temperature for various parts of the echidnas’ bodies (remember, this is done by thermal imaging). The body areas measured are shown in green, and the body temperatures measured at varying wet-bulb temperatures for each body area, are shown as dots, one for each echidna part measured. Measurements were done on 124 echidnas (some may have been duplicates, as they couldn’t identify individuals) at the Dryanra Woodland and Boyagin Nature Reserve in the West Australian wheatbelt, 170 k southwest of Perth, in western Australia:

 

(From paper): Figure 1. Surface temperature of various body regions plotted against wet bulb globe temperature (WBGT) for 124 active short-beaked echidnas (Tachyglossus aculeatus) filmed with an infrared camera in the West Australian wheatbelt. The solid line represents a slope = 1 for WBGT, the dashed line the observed slope for the relationship; asterisks indicate that the slope is significantly different from 1. The inset thermal image shows the body region represented by each panel, outlined with a green polygon.

What you see is that the surface temperature (the height of the dots) is, for six regions of the body, higher than the wet-bulb temperature, which means there’s no evaporative cooling of those warm body surfaces. But look at the “beak tip” at lower right. At all the wetbulb temperatures, the beak tip temperature is the same as the wet-bulb temperature. That means that somehow there is extra cooling going on at the tip of the snout.

How do they do this? They blow snot bubbles out their nose, which, when they burst, keep the nose moist, thus cooling the echidna. In effect, the the beak is a “snot bulb.” Or, to quote the authors:

We identify the beak tip of short-beaked echidnas as a unique type of evaporative window. The beak tip, containing a large dorsal blood sinus, is kept moist to facilitate electroreception. An additional role of this moist surface is evaporative cooling of the underlying blood within the sinus; with a slope equivalent to 1 and minimal intercept, the beak tip functions as a wet bulb globe thermometer. At high Ta [air temperature] echidnas blow mucus bubbles, adding moisture to the beak tip . This unique nasal evaporative window is of particular value for echidnas (which do not pant, lick or sweat) especially under conditions where environmental temperature exceeds Tb [core body temperature] and evaporation is the only avenue available for heat loss.

Here’s a video from Science News about the cooling.  Note that here the lightest areas are the hottest and the darkest are the coolest. Check out the snout tip, circled at 5 seconds in. It’s very dark!

Upshot: Echnidnas have evolved to cool themselves off by blowing snot bubbles when it’s hot. The bubbles’ bursting keeps the animal cool, especially because the snout is well equipped with lots of blood vessels that radiate the heat.

Here’s the authors’ description about how other species use evaporative cooling, including the fact that kangaroos lick their forearms to cool off when it’s hot:

. . . there have been few descriptions for endotherms of specialized evaporative windows where endogenous water is behaviourally applied to areas with specialized vasculature. The classic examples of evaporative windows are for storks and turkey vultures, which urinate on their legs that contain extensive subcutaneous vascularization, facilitating EHL. Seals on rocks similarly urinate to wet their ventral surface and vascularized flippers to enhance EHL, while the licking of vascularized forearms by macropods is the best-known mammalian example.

Storks and seals piss on themselves to cool off! I bet you didn’t know that.

Here’s an Attenborough video of red kangaroos (Osphranter rufus) cooling themselves by licking their highly vascularized forearms (you can skip to 2:05 to see it, as well as thermal images showing the cooling). They also stay in the shade and dig down into the cooler soil beneath the surface and lie down on the cool soil.

 

Now we can add to these examples of evaporative cooling the snot bubbles of echidnas.

h/t Greg Mayer

___________

Cooper C. E. and Withers PC. 2023. Postural, pilo-erective and evaporative thermal windows of the short-beaked echidna (Tachyglossus aculeatus).Biol. Lett.19: 20220495

Flannery, T.F., T.H. Rich, P. Vickers-Rich, T. Ziegler, E.G. Veatch, and K.M. Helge. 2022. A review of monotreme (Monotremata) evolution. Alcheringa 46(1): 3-20.

 

The remarkable physiology of hibernating bears

October 11, 2022 • 10:45 am

Have you been voting in Fat Bear Week? If not, today is the final day: the run-off between two heavyweights that will determine the Fattest Bear.

You probably realize that the bears get so fat in the fall because they are about to go into five months of hibernation, and need to stock up on food to sustain their metabolism as they go into winter. The Washington Post article shown below describes the remarkable phenomenon of hibernation, the potential bodily problems it poses, and new biochemical discoveries that help the bears obviate these issues and could also help immobile humans with the issue of atrophied muscles. Click to read:

Quotes from the article are indented:

But for many scientists, the true fascination of Fat Bear Week involves what happens next, when the now beachball-shaped bruins, carrying about 40 percent body fat, lumber into their dens and start hibernating. During hibernation, they remain healthy under conditions that would weaken and sicken mere humans. The bears emerge months later, lean, strong and barely affected by their months of starvation and inactivity.

Until recently, researchers could not explain how. But several fascinating new molecular studies suggest hibernation remodels bear metabolisms and gene activity in unique and dramatic ways that could have relevance for people. The fat bears can advance our understanding of diabetes, muscle atrophy, inactivity and the ingenuity of evolution.

Superficially, hibernating bears seem passive and inert. For five months or more, they do not eat, drink, urinate, defecate or move, except occasionally to turn over or shiver. Their metabolisms drop by about 75 percent. Hearts beat and lungs inflate only a few times a minute. Kidneys shut down. The bears grow profoundly insulin resistant.

If this were us, we would shed much of our muscle mass because of inactivity and probably develop diabetes, heart disease, kidney failure, frailty and other ills.

But the bears maintain their muscle and rapidly reestablish normal, healthy insulin sensitivity and organ function after hibernation.

Insulin functions to allow cells to absorb glucose from the blood to use as energy, or to convert some glucose to fat. It also helps break down fats and proteins. Normally, the onset of insulin resistance would, as the article implies, lead to diabetes and its attendant problems, but the bears are somehow able to tolerate that—as well as the muscle atrophy attendant on not moving for five months. (Muscle atrophy is a problem for people who are either paralyzed or bedridden for long periods of time.)

How do the bears do this? That’s the point of the article, which links to three scientific articles (one given below) explaining how the bears survive hibernation.

The information on fat usage came from blood samples drawn from hibernating and non-hibernating bears at Washington State University (WSU), bears trained to allow a blood draw without being anesthetized. (I guess the WSU bears also go into hibernation.)

It turns out that there is differential activation of genes in the bears during hibernation that protect them from deleterious effects of hibernation. Here are two papers cited:

By comparing the samples, [reserachers] concluded hibernation is biologically uncanny but hardly quiet. In a 2019 study, the WSU scientists and others found more than 10,000 genes in bears that work differently during hibernation vs. in autumn or spring. Many involve insulin activity and energy expenditure and most occur in the animals’ fat, which becomes quite insulin resistant during hibernation and robustly insulin sensitive immediately afterward.

Digging deeper into that process for a new study, published in September in iScience, they bathed fat cells drawn from hibernating and active bears with blood serum taken during the opposing time and watched the fat switch seasons. Fat from hibernating bears became insulin sensitive and genetically similar to fat from the active season and vice versa.

In other words, something in the blood serum of non-hibernating bears restored the insulin sensitivity of hibernating bears, and vice versa. This shows that it is something in the serum, and not in the fat, that changes during hibernation. The article continues:

Perhaps most compelling, they also identified and cross-matched hundreds of proteins in the animals’ blood and found eight that differed substantially in abundance from one season to the next. These eight proteins seemed to be driving most of the genetic and metabolic changes in the fat.

Of course correlation is not causation, and I doubt that 10,000 genes are involved in actually producing hibernation or mitigating its effects. (After all, humans have only about 25,000 protein-coding genes—more if you include as “genes” bits of DNA that do something but don’t produce proteins—and bears can’t differ that much from us. There may be changes in that many genes, but many of these may simply be side effects of natural selection changes the expression of many fewer genes.

But it’s clear that genes involved in insulin usage and sensitivity work differently in hibernating versus nonhibernating bears. What are the cues that turn these genes on and off? I doubt that we know, and the paper doesn’t say, but a good guess is that this has to do with environmental factors indicating the impending arrival of spring or fall: cues based on day length or temperature.

But what about the bears’ muscles? Why don’t they atrophy? Again, it’s due (as it must be) to differential activation of genes. And again, the gene products responsible seem to be circulated in the blood serum.

The paper below from PLoS ONE (click on screenshot to read; pdf here and reference at bottom), implicates both the blood serum and the genes involved in maintaining muscle.

The Japanese researchers bathed cultured human skeletal muscle cells in serum from either hibernating or non-hibernating black bears. What they found was significantly less degradation of protein when hibernating-bear serum was used. This appeared to be based on a gene-induced decrease in levels of two proteins and an increase in the level of another, which act in concert to preserve protein levels in the cultured cells. (The protein made in reduced amount breaks down muscle while the others promote and sustain muscle growth.) Altogether, changes in gene action appears to keep the bears’ muscles fairly intact as they go through hibernation.

Now these are cultured human cells, not bear cells, and the experiment was done in vitro rather than in vivo, but it gives a very promising lead to how bears keep their muscles strong during hibernation.

The Post article also lays out the potential uses of this information in human health.

Fat.

Potentially, these same eight proteins, which also appear in human blood, might at some point be harnessed pharmaceutically to improve insulin sensitivity or treat diabetes and other metabolic disorders in people, Kelley said. But that possibility lies far in the future and requires vastly more research with bears and us (although perhaps not in close proximity).

Muscle.

The ultimate aim of this research, [author] Miyazaki said, is to isolate and refine all of the substances and processes in hibernating bears’ blood and elsewhere in their bodies that protect them from muscle wasting, with the hope that these same elements might treat atrophy from bed rest or aging in people.

“There is probably no better way to maintain a healthy lifestyle than through physical exercise,” he said, but for people who cannot be active, for whatever reason, the internal operations of slumbering bears might someday provide respite from frailty.

It’s important to remember that these remarkable changes are certainly due to evolution via natural selection, as it’s hard to imagine a random process like genetic drift causing evolutionary changes that are certainly adaptive.

As Ernst Mayr emphasized, many important evolutionary changes in animals begin with a change in behavior. Perhaps bears in cold areas survived better if they underwent a period of low activity during winter when food is scarce (this behavioral change could reflect genetic variation), and then those quiescent bears who also had mutations affecting fat and muscle metabolism would be those most likely to survive hibernation, leaving their genes to future bear generations.

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Miyazaki M, Shimozuru M, Tsubota T. (2022) Supplementing cultured human myotubes with hibernating bear serum results in increased protein content by modulating Akt/FOXO3a signaling. PLoS ONE 17(1): e0263085. https://doi.org/10.1371/journal.pone.0263085

It’s Nobel Prize Week! Physiology/Medicine Prize awarded to pair for work on bodily temperature and touch sensors. Plus, our annual Guess-the-Laureate Contest.

October 4, 2021 • 8:45 am

Starting today and extending for a week, we’ll have a Nobel Prize awarded every weekday. The Physiology or Medicine Prize was announced this morning in Stockholm, and so two investigators will have been woken up early but will be very happy. Here they are with some info from the Howard Hughes Medical Institute (I’ve added links):

David Julius [left below], a professor at the University of California, San Francisco and a Howard Hughes Medical Institute (HHMI) Trustee, and Ardem Patapoutian [right], an HHMI Investigator at Scripps Research have received the award for their work identifying receptors on sensory neurons that give us the ability to monitor temperature, pain, touch, and movement of our body.

The prize was announced here and the explanation of what Julius and Patapoutian found is here or at the HHMI site.  Trigger warning: Hot peppers are involved! Here’s the official announcement (32 minutes), which gives the names and explains the discoveries as well with the explanation beginning at 2:23.

A tweet sent mr by Matthew:

Because the biology prize was announced already, it can’t be part of our annual contest to “Guess the Laureates”. Since nobody ever wins that one, I’m making it easier this year.

Look at the announcements below, and then guess the names of ONLY THREE LAUREATES, one from each of three of the five categories of your choice: physics, chemistry, literature, peace, or the economics prize. If there you have multiple guesses in a category, you can guess only one recipient. 

Remember: just give me three names and the area in which each is supposed to win. 

If you guess a name after the prize is awarded, your entry doesn’t count. So if you’re guessing in physics, your deadline is this evening, and so on.

If there is more than one winning entry (all three guesses correct), we will have a raffle for the winner. The Coyne Prize is, also as usual, an autographed copy of one of my two trade books (WEIT or Faith Versus Fact), with a picture drawn in (by me) of an animal of your choice.  I suggest that you enter (in the comments below) by the end of today.

***************

Here’s the schedule of announcements from the organization itself:

AWARDED: PHYSIOLOGY OR MEDICINE – Monday 4 October, 11:30 CEST at the earliest
The Nobel Assembly at Karolinska Institutet, Wallenbergsalen, Nobel Forum, Nobels väg 1, Solna
http://www.nobelprizemedicine.org
nobelforum@nobelprizemedicine.org

PHYSICS – Tuesday 5 October, 11:45 CEST at the earliest
The Royal Swedish Academy of Sciences (Kungl. Vetenskapsakademien, KVA), Sessionssalen, Lilla Frescativägen 4A, Stockholm
www.kva.se/pressroom
eva.nevelius@kva.se

CHEMISTRY – Wednesday 6 October, 11:45 CEST at the earliest
The Royal Swedish Academy of Sciences, Sessionssalen, Lilla Frescativägen 4A, Stockholm
www.kva.se/pressroom
eva.nevelius@kva.se

LITERATURE – Thursday 7 October, 13:00 CEST at the earliest
The Swedish Academy (Svenska Akademien), Börssalen, Källargränd 4, Stockholm
http://www.svenskaakademien.se/en
louise.hedberg@svenskaakademien.se

PEACE – Friday 8 October, 11:00 CEST
The Norwegian Nobel Committee, The Norwegian Nobel Institute (Norska Nobelinstitutet), Store Sal, Henrik Ibsens gate 51, Oslo
https://www.nobelpeaceprize.org
postmaster@nobel.no

THE SVERIGES RIKSBANK PRIZE IN ECONOMIC SCIENCES IN MEMORY OF ALFRED NOBEL – Monday 11 October, 11:45 CEST at the earliest
The Royal Swedish Academy of Sciences, Sessionssalen, Lilla Frescativägen 4A, Stockholm
www.kva.se/pressroom
eva.nevelius@kva.se

Are sponges the closest relatives of the rest of the animals?

March 21, 2021 • 9:30 am

A new paper in Nature Communications highlights an ongoing controversy in the evolution of animals: what are the closest relatives of living multicellular animals?

First, though, we need to refresh ourselves on what “animals” are. Merriam-Webster defines them adequately:

Any of a kingdom (Animalia) of living things including many-celled organisms and often many of the single-celled ones(such as protozoans) that typically differ from plants in having cells without cellulose walls, in lacking chlorophyll and the capacity for photosynthesis, in requiring more complex food materials (such as proteins), in being organized to a greater degree of complexity, and in having the capacity for spontaneous movement and rapid motor responses to stimulation.

We’re leaving out the single-celled “animals” here (under “outgroups” in the figure below) and concentrating on multicellular animals.

The multicellular animals include (as the phylogenies show below), Ctenophores, or comb jellies, Porifera (sponges), Placozoans (free living but small multicellular organisms), Cnidaria (corals, jellyfish, sea anemones and their relatives), and Bilateria (everything else; all animals with a head and tail end, as well as a belly and a back at some stage of their life, including echinoderms which have these features as larvae).  Over the years, a combination of developmental, morphological, and molecular analysis has given rise to the two conflicting family trees shown below.

Both trees are the same except for a dispute about the “animal outgroup” (the “breakaway group” or “sister group”), the closest living relative to the vast bulk of the animals, and the first group to branch off from the rest. One school, shown on the left, adheres to the ctenophores, or comb jellies, as this sister group. The other, shown on the right, maintains that sponges occupy this position, and ctenophores branched off later.

 

Here’s an example of a ctenophore (photos from Wikipedia):

And a bunch of sponges:

Now the case for sponges as the sister group is based on the observation that ctenophores share unique features with the other animals, including elements of nervous systems, and (except for Placozoans) muscles and a tubelike digestive system (“gut”). But sponges have none of these. Moreover, sponges are made up of collared cells, or choanocytes, which are similar to “choanoflagellates“, singled-celled protozoans thought to be the closest relative to all the animals from sponges on down. This similarity implies that the common ancestor of multicellular animals might have been something spongelike, supporting the second phylogeny above. That implies that sponges changed relatively little after multicellular animals evolved, while everything else changed a lot more.

But some molecular phylogenies have suggested that the more complex ctenophores might be the outgroup instead of sponges.  This is a bit more problematic to both me and Matthew (see his BBC broadcast below), for if sponges are really more closely related to other animals than are ctenophores, why do ctenophores have muscles, nerves, and an in—>out digestive system like most other animals, but sponges lack these things? To hold that ctenophores are the sister group instead of sponges requires that you posit one of two possibilities:

A.) The common ancestor of all animals had nervous systems and muscles and a gut, which persist in all groups but the sponges, and the sponges lost these features. That seems unlikely, but it’s possible.

or

B.) The common ancestor of all animals lacked these features, but they evolved independently in the choanoflagellates and all other animals save sponges. This seems even more unlikely since it requires the independent evolution of three complex traits in two separate groups (ctenophores and [other animals minus sponges]).

This principle of “parsimony” alone suggests that sponges are the sister group, didn’t lose any of those features, and muscles, nerves, and a gut evolved only once.

The new article in Nature Communications supports the “sponges first” scenario. Click on the screenshot below to read the article, see the pdf here, and find the reference at the bottom of this post. The authors used a new way of making phylogenies using DNA data, dubbed “partition site-heterogeneous models” to eliminate artifacts that may have erroneously shown ctenophores as the sister group of other animals. I’m not going to explain that method and, to be sure, I don’t understand it. In fact, the main results of the paper for the layperson can be described very simply: the new method shows that sponges are the sister group to all animals, a result that makes sense.

I just gave you the punch line, but have to add that the controversy isn’t settled. It is settling, however, as more and more biologists come around to the “sponges split off first” scenario. (I won’t even mention the controversy about the placozoans and ctenophores, and where they fit with relationship to Cnidaria.) Let me just put in the authors’ paragraph where they say that their finding of sponges as the sister group of all other animals is definitive: (my emphasis):

Several studies have already shown that gene family and unpartitioned phylogenomic analyses using more sophisticated substitution models reject Ctenophora sister in favour of Porifera sister. Here, we have consolidated these findings by directly showing that the primary remaining lines of evidence supporting Ctenophora sister, partitioned phylogenomics and measures of underlying support (such as ΔPSlnl values), do not do so when better-fitting site-heterogeneous models are incorporated into the analysis. Thus, the Ctenophora-sister hypothesis can now be wholly rejected in favour of the traditional Porifera-sister scenario of animal evolution, wherein the animal ancestor did not possess key traits such as a nervous system, muscles or a mouth and gut.

Ctenophores as the sister group is now “wholly rejected”! I suspect that not all animal systematists would accept this hypothesis. I do, tentatively, but I don’t fully understand the complex methods of analyzing DNA data (they used 60 animal groups, 406 genes, and 88,384 DNA sites).  My view of these complex methods is the same one that my academic grandfather, Theodosius Dobzhansky, held towards the experts in mathematical population genetics (Dobzhansky was innumerate): “Papa knows best.”

For a fuller explication of the conflict, as well as an overview of animal evolution in general, you can’t do better than Matthew’s 2018 Discovery PROGRAM on the BBC. The controversy about sponges-first versus ctenophores-first starts at 17:45. This program is very good, involves interviews with a lot of different biologists, and should be very clear to the sentient layperson. Plus it’s only half an hour long. Spend this Sunday learning a bit about animal evolution!

Click on the screenshot to hear the show:

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Redmond, A.K., and A. McLysaght 2021. Evidence for sponges as sister to all other animals from partitioned phylogenomics with mixture models and recoding. Nat Commun 12, 1783 (2021). https://doi.org/10.1038/s41467-021-22074-7

Nobel Prize for Physiology or Medicine goes to three for discovering the Hepatitis C virus

October 5, 2020 • 7:00 am

Knowing that the first Nobel Prize for science would be awarded today—in Physiology or Medicine—I made a contest in which readers were to guess just one winner of each of the three science prizes plus the winner of this year’s Literature Nobel.

Well, the first prize was awarded this morning, and the contest is already over. Everyone lost (see here and here).

Granted, this was not an easy one to guess. The award in fact went to three people—Harvey Alter, Michael Houghton, and Charles Rice—with each getting a third of the prize money. The award was given for the discovery of the virus that causes Hepatitis C.  Here’s part of the press release from the Nobel Prize site:

This year’s Nobel Prize is awarded to three scientists who have made a decisive contribution to the fight against blood-borne hepatitis, a major global health problem that causes cirrhosis and liver cancer in people around the world.

Harvey J. Alter, Michael Houghton and Charles M. Rice made seminal discoveries that led to the identification of a novel virus, Hepatitis C virus. Prior to their work, the discovery of the Hepatitis A and B viruses had been critical steps forward, but the majority of blood-borne hepatitis cases remained unexplained. The discovery of Hepatitis C virus revealed the cause of the remaining cases of chronic hepatitis and made possible blood tests and new medicines that have saved millions of lives.

. . . The Nobel Laureates’ discovery of Hepatitis C virus is a landmark achievement in the ongoing battle against viral diseases (Figure 2). Thanks to their discovery, highly sensitive blood tests for the virus are now available and these have essentially eliminated post-transfusion hepatitis in many parts of the world, greatly improving global health. Their discovery also allowed the rapid development of antiviral drugs directed at hepatitis C. For the first time in history, the disease can now be cured, raising hopes of eradicating Hepatitis C virus from the world population. To achieve this goal, international efforts facilitating blood testing and making antiviral drugs available across the globe will be required

Here’s the video of the award with details about the winners, and giving some scientific background; the action starts at 12:50. It’s worth listening to the 20 minutes of science, as you’ll learn a lot. There’s also an interview with the Secretary of the Prize Committee beginning at 34:34.

I guess the prize for CRISPR-Cas9 will have to wait for another year.